Physiology - An Illustrated Review (eBook)
352 Seiten
Thieme Medical Publishers (Verlag)
978-1-63853-315-3 (ISBN)
Introducing Thieme's illustrated Review SeriesConcise course reviews that also test your knowledge for the USMLE!Thieme's illustrated Review Series serves an important dual purpose for medical studentsboth concise course review and high-yield USMLE(R) test preparation. Covering all the basic science subjects that you will take in medical school and that will be found on the USMLE(R) Step 1, the series features unparalleled color illustrations, a streamlined format, and hundreds of print and online study questions and answersall designed to increase your mastery of the topics, promote classroom success, and boost your confidence for the exam!PhysiologyAn Illustrated Review helps you master the important physiologic facts and concepts, organized by organ system, and teaches you how to apply that knowledge for classroom and USMLE(R) success. This indispensable review book includes:Hundreds of beautifully detailed, fully labeled color illustrations that clarify each conceptA succinct, bullet-point format that focuses on must-master classroom and exam informationHandy sidebars that integrate key content across the basic science curriculum and demonstrate clinical correlationsClear tables that summarize topics and provide easy-to-study review200 USMLE(R)-style and factual self-testing questionswith explanatory answersthat give you intensive practice in each areaAn additional 200 interactive questions and answersfor a total of 400are available online via the scratch-off code in your book, offering immediate feedback and quickly identifying areas for further study
2 Neurotransmission
Propagated action potentials carry information through axons over long distances, but they do not transfer electrical impulses directly to other neurons, glands, or muscle cells. Communication between most nerve cells is accomplished via neurotransmitter molecules released at synapses.
2.1 Neurotransmitters
Acetylcholine
Synthesis. Acetylcholine is synthesized from acetyl coenzyme A (CoA) and choline by the enzyme choline acetyltransferase in the presynaptic terminal. The uptake of choline is the rate-limiting step.
Coenzyme A
Pantothenic acid (vitamin B5) is a precursor of CoA. CoA participates in fatty acid synthesis and oxidation, as well as the oxidation of pyruvate in the citric acid cycle. A molecule of CoA that has an acetyl group is referred to as acetyl CoA. Acetate, which is derived from acetyl CoA, combines with choline to form the neurotransmitter a cetylcholine.
Degradation. Breakdown is rapid via acetylcholinesterase to produce acetate and choline. Acetylcholinesterase is located on neuronal membranes, muscle cell membranes, and red blood cells. Pseudocholinesterases (nonspecific) and butyrylcholinesterases, which are more widely distributed, can also hydrolyze acetylcholine.
Release. Acetylcholine is the neurotransmitter released from the following neurons (see also page 35 and Fig. 4.1):
– Pre- and postganglionic parasympathetic neurons
– Preganglionic sympathetic neurons
– Postganglionic sympathetic neurons that innervate sweat glands
– Motoneurons at the neuromuscular junction
Norepinephrine
Synthesis. Norepinephrine is synthesized from the precursor amino acid tyrosine by hydroxylation to dihydroxyphenylalanine (dopa) in the postganglionic neuron. Dopa is decarboxylated to dopamine, which is oxidized to norepinephrine and packaged in vesicles.
Degradation. Termination of action is primarily by reuptake (60–90%) into nerve terminals. Secondary degradation is by monoamine oxidase (MAO) and catechol O-methyltransferase (COMT).
Monoamine oxidase inhibitors
Monoamine oxidase inhibitors (MAOIs, e.g., isocarboxazid and phenelzine) inhibit both forms of the enzyme monoamine oxidase (MAO-A and MAO-B). In doing so, they prevent the degradation of norepinephrine, epinephrine, and dopamine. These drugs are used in the treatment of depression when tricyclic antidepressants are in effective. It takes 2 to 3 weeks for the desired effects of these drugs to occur.
Hypertensive crisis with monoamine oxidase inhibitors
Hypertensive crisis may occur within hours of ingestion of tyramine-containing foods, including cheese, certain meats (liver and fermented or cured meats), cured or pickled fish, overripe fruits and vegetables, Chianti wine, and some beers. Hypertensive crisis is characterized by headache, palpitation, neck stiffness or soreness, nausea, vomiting, sweating (sometimes with fever or cold, clammy skin), photophobia, tachycardia or bradycardia, constricting chest pain, and dilated pupils. Potentially fatal intracranial bleeding may result from this crisis. Patients should avoid tyramine-containing foods while taking MAOIs and for 2 weeks after treatment with MAOIs is discontinued to avoid precipitating this condition, but if it does occur, then treatment is with intravenous phentolamine.
Release. Norepinephrine is the main neurotransmitter released from postganglionic sympathetic neurons. It is also released in small quantities from the adrenal medulla along with epinephrine.
Epinephrine
Synthesis. Epinephrine is produced from norepinephrine in the adrenal medulla via the enzyme phenylethanolamine N-methyltransferase.
Degradation. Epinephrine is degraded by MAO and COMT.
Release. Epinephrine is released from the adrenal medulla along with some norepinephrine.
Dopamine
Synthesis. Dopamine is a precursor in the formation of both norepinephrine and epinephrine.
Degradation. Dopamine is degraded by MAO and COMT.
Release. Dopamine acts as a neurotransmitter in the central nervous system (CNS), especially in the extrapyramidal motor system.
Glutamate
Synthesis. Glutamate is synthesized from glucose via glutamine.
Degradation. Glutamate is converted back to glutamine, and its action is terminated by reuptake into cells in the CNS.
Release. Glutamate is the principal excitatory amino acid neurotransmitter in the CNS.
Gamma-Aminobutyric Acid
Synthesis. Glucose is the principal in vivo source of gamma-aminobutyric acid (GABA). There is a GABA “shunt” of the Krebs cycle that results in the conversion of glutamate into GABA by the action of the enzyme glutamate decarboxylase.
Degradation. GABA is converted back to glutamate, then to glutamine. Its action is terminated by reuptake into cells in the CNS.
Release. GABA is the principal inhibitory amino acid neurotransmitter in the CNS.
Serotonin
Synthesis. Serotonin (5-hydroxytryptamine [5-HT]) is synthesized from tryptophan by tryptophan hydroxylase.
Degradation. Serotonin is degraded by MAO.
Release. Serotonin acts as a neurotransmitter in the CNS.
Carcinoid syndrome
Carcinoid tumors are neuroendocrine tumors of the gastrointestinal (GI) tract, urogenital tract, or pulmonary bronchioles. They can contain and secrete numerous autocoids, including prostaglandins and serotonin, causing symptoms such as flushing and diarrhea. Cardiac disease due to fibrosis of the endocardium and valves, along with asthma-like symptoms, are also common. Flushing may be precipitated by stress, alcohol, certain foods, or drugs, particularly serotonin-specific reuptake inhibitors (SSRIs), so these should be avoided. Heart failure, wheezing, and diarrhea are treated, respectively, with diuretics, a bronchodilator, and an antidiarrheal agent, such as loperamide or diphenoxylate. If patients remain symptomatic, serotonin receptor antagonists, antihistamines, and somatostatin analogues are the drugs of choice. 5-HT3 receptor antagonists (ondansetron, tropisetron, dolasetron, granisetron, palonosetron, ramosetron, alosetron, and cilansetron) can control diarrhea and nausea and occasionally ameliorate the flushing. A combination of histamine H1 and H2 receptor antagonists (diphenhydramine and cimetidine or ranitidine) may control flushing in patients with upper GI or pulmonary carcinoids. Synthetic analogues of somatostatin (octreotide and lanreotide) are the most widely used agents to control the symptoms of patients with carcinoid syndrome.
Glycine
Synthesis. Glycine is the simplest amino acid.
Degradation. Glycine is broken down by glycine dehydrogenase.
Release. Glycine is released by the inhibitory interneurons in the spinal cord that are activated by group Ia muscle afferents (see page 65). It acts by increasing Cl− conductance in the postsynaptic membrane, hyperpolarizing it, and thus preventing action potential generation.
Histamine
Synthesis. Histamine is synthesized from histidine by histidine decarboxylase.
Degradation. Histamine is degraded by MAO.
Release. Histamine acts as a neurotransmitter in the CNS.
Nitric Oxide
Synthesis. Nitric oxide (NO) is not stored in vesicles. It is synthesized as required in the pre-synaptic terminal from arginine by the enzyme NO synthase.
Degradation. NO has a half-life of only a few seconds.
Release. NO acts as an inhibitory neurotransmitter in the CNS, GI tract, and blood vessels.
Table 2.1 provides examples that are predominantly excitatory or inhibitory.
2.2 Synaptic Transmission
Presynaptic Events
An action potential depolarizes the presynaptic terminal cell membrane, causing membrane Ca2+ channels to open and Ca2+ influx into the presynaptic terminal. This Ca2+ influx then stimulates the release of neurotransmitters from storage vesicles into the synaptic cleft (Fig. 2.1).
Fig. 2.1 Synaptic signal transmission.
An action potential (AP) arriving at the presynaptic membrane (1) causes voltage-gated Ca2+ channels to open (2). This increase in intracellular [Ca2+] triggers the release of neurotransmitters from their storage vesicles into the synaptic cleft (3). Neurotransmitter molecules then diffuse across the synaptic cleft (4) and bind with inotropic or metabotropic receptors on the postsynaptic membrane. Inotropic receptors are ligand-gated ion channels. Ligand (in this case, neurotransmitter) binding (5) causes the inflow of ions into the cell, resulting in either depolarization (inflow of cations) or hyperpolarization (inflow of anions). (6) Ligand binding to metabotropic receptors activates G proteins, which transduce a cellular response via second messenger...
| Erscheint lt. Verlag | 10.10.2011 |
|---|---|
| Reihe/Serie | Thieme Illustrated Reviews | Thieme Illustrated Reviews |
| Sprache | englisch |
| Themenwelt | Medizin / Pharmazie ► Medizinische Fachgebiete |
| Studium ► 1. Studienabschnitt (Vorklinik) ► Physiologie | |
| Naturwissenschaften ► Biologie | |
| Schlagworte | Illustrated • Illustrations • Physiology • Review |
| ISBN-10 | 1-63853-315-6 / 1638533156 |
| ISBN-13 | 978-1-63853-315-3 / 9781638533153 |
| Haben Sie eine Frage zum Produkt? |
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